The basic tool of BLS oxygenation is the bag-valve-mask, aka the bag-mask (as the AHA calls it), aka the Ambu-Bag (as most in-hospital staff call it, after one of the popular manufacturers), aka the self-inflating resuscitator. We’ll talk about techniques for optimizing for BVM success later. For the moment, let’s discuss some of the other auxiliary aids available. As we do, remember our main challenges: if we don’t minimize the resistance to airflow into the trachea, we’ll be prone to inflating the stomach instead of the lungs. And if we don’t minimize obstructions higher in the pharynx, we won’t be able to introduce any air at all.

Nasopharyngeal and Oropharyngeal airways

The NPA (or nasal trumpet) and OPA are the mainstays of BLS airway adjuncts. Essentially, they’re just curved pieces of plastic or rubber, designed to be inserted into the upper airway to prevent soft tissue from collapsing and obstructing the lumen.

When I first learned about these, it was just after hearing about the head-tilt chin-lift and jaw thrust, which were purportedly enough to open any self-obstructing airway. Why did we need these tools? “This way,” my instructor advised, “you don’t have to sit there holding their airway open.”

Well, yes and no.

The standard theory behind these devices is this: in a supine, unconscious patient, the tongue (and other soft tissue) wants to collapse into the pharynx. If we can jam something in the way, it will essentially “splint” open the passage — stick a foot in the door — much as if we were holding tissue back with a tongue depressor. Positioning the head and neck in such a way that it widens the relevant gaps would accomplish the same thing.

Under this thinking, we have several redundant tools to accomplish the same purpose. Whether we open the airway by tilting their head and lifting their jaw, or by sticking an OPA in the mouth, or by sticking an NPA in the nose, the result is the same.

But this doesn’t quite reflect reality. Sometimes it will, but in many patients with difficult airways, it’s not so simple to maintain a patent passage for airflow. In an obese patient with challenging upper airway anatomy, the amount of soft tissue standing in your way may be profound, and it can obstruct the lumen in multiple places. Additionally, tone may be so lacking that it easily “molds” around anything you stick in there.

In other words, if you place a BLS airway, the only breathable passage you’re really guaranteed is the lumen enclosed by the device itself: the central hole or grooves. And that’s not very much room. Our goal isn’t to create a tiny breathing tube, it’s to maximize the amount of usable airway — we’d like to be able to ventilate through as large a diameter as possible. That means using everything we can.

So proper positioning is helpful. So is an OPA. And perhaps an NPA. Or two.

In fact, if at all possible, it’s always worth trying to insert multiple airways. This is typically not taught to EMTs (since textbooks subscribe to the the “splinting” rather than the “protected lumen” theory), but it’s widely practiced in the ED and by experienced paramedics. If you’re having any difficulty at all bagging, shoot for an OPA with bilateral NPAs; filling all the available holes with patent airways is always a good idea.

Remember what you’re actually doing with each airway. With an NPA, you’re separating the soft palate from the superior and posterior nasopharynx, and if it’s properly sized, it should be long enough to create a passage through the laryngopharynx, nearly to the epiglottis. (If it’s too long, it can stimulate the gag reflex, or jam into the vallecula or epiglottis, actually obstructing the larynx; if it’s too short, it may not protect the laryngopharnyx, or even may not fully span the nasopharynx, allowing the soft palate to shut.) With an OPA, you’re separating the lips, depressing the tongue to prevent it from obstructing the oral cavity, and more importantly protecting the laryngopharynx in the same way the NPA does — keeping the tongue or other anterior structures clear.

So if you only insert an NPA, the nose is your only guaranteed airway. If the mouth itself is shut — and we typically squeeze it shut when we bag using the “EC clamp” technique — nothing will flow through the oropharynx. Conversely, if we only insert an OPA, there is no guarantee that the nasopharynx will remain patent, particularly where the soft palate wants to meet the posterior pharynx.

So use both, because we want it all.

OPAs are more widely used, but it’s a shame to neglect the NPA. The advantage, of course, is that patients with an intact gag reflex can still tolerate an NPA, whereas the OPA may stimulate vomiting. It’s unwise to use the “try and see” approach with the OPA, because there’s nothing quite like copious emesis to make a difficult airway more difficult. Kyle David Bates teaches the helpful tip of inspecting for saliva and secretions collecting in the mouth; if there are none, the patient likely has an intact gag reflex. If they are present, an OPA is probably safe. But suction is always worth keeping on-hand and prepared.

It’s taught that NPAs are contraindicated in patients with significant facial or cranial trauma, on the theory that you may pass the device through a basal skull fracture right into the brain. This is probably a negligible risk; the entire concept seems to be based on two (yes, that’s the number before three) case reports in the literature. If your suspicion is quite high (blood from the nose with a positive halo test, for instance), you may want to steer clear, but with a truly difficult airway, remember that oxygenation is more important than an extremely remote risk of poking the patient’s noodle.

NPA placement can be facilitated by ensuring you lubricate the device first (water-based jelly should be available, although traditionally the patient’s saliva can be used as a last resort), aiming “in” (posteriorly) rather than “up” (superiorly), and lifting the nose to facilitate this angle. Also, remember that each nasal fossa has erectile tissue which takes turns engorging and partially obstructing airflow (allowing cyclical “resting” of the mucosa), so at any given time, one nare will likely allow easier NPA passage than the other; if you’re having difficulty, just switch sides. (Stripping part of this tissue away from the concha will occasionally cause post-insertion bleeding, but it’s rarely significant.)

As for the OPA, we usually teach insertion with the tip pointing up, followed by a 180-degree rotation once it’s fully inserted. Just remember that it’s also acceptable and sometimes easier to insert it tip-down while holding back the tongue with a tongue depressor or finger.

Another somewhat prosaic benefit to the OPA is that it may help provide structure to edentulous [toothless] patients when you’re trying to bag them, although simply leaving dentures in place can also work.

Apneic Oxygenation

You may not think that the lowly nasal cannula and non-rebreather mask really qualify as useful airway tools in an apneic patient. But oh, you would be wrong.

Pop quiz: is it possible to oxygenate the blood without actively moving any air? In other words, can you breathe without breathing?

You might say no. But why not? Gas exchange in the alveoli is not an active process; you’re not forcing the O2 molecules across the membrane by any chemical or muscular exertion. They simply diffuse passively, like gin dispersing into your tonic. All you’re doing when you breathe (either spontaneously or via positive-pressure ventilation) is providing a fresh supply of air to ensure that the concentration of oxygen in the alveoli remains higher than the concentration in the blood (thus allowing diffusion to occur). If we can keep the alveolar oxygen levels high without breathing, that’s just fine.

Suppose, for instance, that we place the apneic patient on a nasal cannula at relatively high flow. This should fill the pharynx with near-100% O2. Even without breathing, gas exchange is occurring in the alveoli; oxygen is diffusing across the membrane into the blood where it binds hemoglobin, and carbon dioxide is diffusing the opposite direction. Far less CO2 is moving out than oxygen is moving in, however (due to differences in solubility and hemoglobin affinity), so there’s actually a net “loss” of gas. This creates some “suction” or a partial vacuum in the alveoli, which will draw in whatever gas is waiting in the upper airway to fill it. Since we’ve flushed that space with pure O2, oxygen will move down that gradient, enter the alveoli, and continue diffusing into the blood, creating a continuous flow. Using this method, patients have been demonstrated to maintain reasonable sats for ridiculously long periods (up to 100 minutes in ideal circumstances).

This is a technique called apneic oxygenation. Although referred to by different names, it’s not new (among other things, it’s a traditional component of most brain-death evaluations), but it’s recently been getting more publicity. In particular, Scott Weingart of EMcrit and Richard Levitan recently published a paper comprehensively describing its use in difficult intubations. They advise placing a cannula at 15 L/min in order to suffuse the pharynx with near-100% O2, and this recommendation has some support in the literature. (Interestingly, whether the patient has their mouth open or closed may not matter.) We’re usually taught that nasal cannulae shouldn’t be used at flows this high, since it’ll dry and irritate the mucosa of the nose, and this is true; however, for short periods in critical patients, a dry nose is not the foremost concern.

How could this be useful for our purposes? Our main challenge with the BVM is ensuring that positive pressure goes where we want it to. This is obviously essential. But if bagging is initially challenging, could we potentially buy time? As long as the airway down to the glottis is open to flow, at least partially, it takes no skill at all to place a cannula (probably already present) and run up the flow to 15 L/min. Even if we’re totally unable to ventilate effectively, this will help keep the patient oxygenated and saturated while we work on a more definitive solution.

A couple of caveats: first, there must actually be a somewhat patent (if not totally secure) airway for this to work. If upper airway structures (or even a foreign body) have totally occluded the nasopharynx or laryngopharynx, no oxygen will reach the trachea. Second, this is a short-term temporizing measure only, because although it may help oxygenate, it will not help to “ventilate,” meaning to remove waste carbon dioxide; as discussed, CO2 is much less capable of passively diffusing without actual tidal movement to clear the alveolar space. Sustained apnea will therefore lead to continually increasing hypercapnia. Finally, this is really intended for patients with largely normal V/Q ratios; it will probably be of limited use for patients with significant shunt (e.g. bronchoconstriction, pulmonary edema, etc.) or dead space (e.g. pulmonary embolism). In other words, it’s of little help to your respiratory patients, whose problem is that their lungs aren’t working properly; if they’re moving air at all, they’re most likely suffusing their alveoli with high-concentration O2, it’s just that they’re just unable to exchange it. They need something like CPAP to help recruit more usable alveoli. Apneic oxygenation is for patients with working lungs who merely aren’t breathing spontaneously or adequately protecting their airway.

Can’t you just use a mask for this? Eh. Studies suggest that O2 from a non-rebreather tends to remain outside the face (in the bag and mask itself) unless the patient actually breathes, since it’s easier for the gas to simply overflow from the exhalation ports than to penetrate their airway; this is distinguished from the cannula, which actually shoots pressurized oxygen directly into the nasopharynx.

However, when it comes to patients who do still have some spontaneous respirations, a non-rebreather can certainly be useful, and here’s a way to supercharge it. Contrary to popular belief, you’re not actually delivering 100% oxygen with a typical mask at 15 L/min — more like 60–70% in most cases. This is due both to the poor seal it generally forms with the face and to the fact that at least one external port is usually left open to room air, so that if the oxygen supply is interrupted or becomes inadequate the patient won’t be suffocated. However, you can get closer to 100% FiO2 by simply cranking up the flow. Once you hit around 30–60 L/min, enough surplus oxygen is overflowing through the mask that the patient should be breathing nearly pure O2. Your portable oxygen tank probably won’t allow a flow this high (and it’d quickly run empty if it did), but most wall- or ambulance-mounted regulators should, although it may be near their maximum flood. Just crank the regulator up to 15 and keep turning until it won’t turn anymore; the indicator won’t change, but the flow will keep increasing. (Although I won’t be the one to recommend it due to the [likely overstated] safety concerns, you could probably also get good results by taping over any valveless ports in the mask, and holding it tightly sealed to their face — or better yet, letting them hold it.)

It may seem convenient, incidentally, to simply press a BVM against their face. Although this may — may — produce an effective seal, it provides poor O2 flow for spontaneous respirations; often times patient-initiated breaths simply bypass the reservoir and draw room air.

Key Points

When it comes to BLS airway adjuncts, the more the better. Two NPAs and an OPA is ideal.

NPAs are generally safe; the risk of penetrating the cranial vault is probably negligible.

Don’t go poking around with the OPA in already-difficult airways; make an effort to determine whether a gag reflex is present before stimulating it.

If an open airway to the lungs exists, but ventilations are difficult, a nasal cannula at 15 L/min is an excellent way to provide apneic oxygenation as a temporizing measure to maintain saturation.

The only “high-flow” oxygen device on your ambulance for a spontaneously-breathing patient is a non-rebreather with flow of 30+ L/min.

A general reminder: although we are cavalier with failing to include in-line or footnoted citations, these are all evidence-based recommendations, and readers are encouraged to inquire for the literature behind anything that seems surprising or dubious.

Sometimes, patients can’t breathe. When that happens, we need to breathe for them.

Simple enough. This is life support at its most fundamental, and many of the interventions classified as “BLS” are found here — techniques and devices for artificially supporting the body’s airway and breathing.

And it doesn’t seem so hard. When they taught it in class, it only took a day or two, and a few pages in the textbook encompassed the subject. How to size an OPA, how to hold the BVM, something about jaw thrusts, and you’re through. Spend a few minutes playing with a mannequin and now you’re an expert.

In the real world, though, this is not child’s play. Managing the airway of a sick, apneic patient is, at best, a high priority; at worst, it’s an unqualified catastrophe. Case reports and horror stories of airways gone wrong can be found under every roof: the failed intubation, the disastrous cricothyrotomy, the foreign body obstruction that couldn’t be cleared. These are emergencies because as we all know, without an airway, you cannot survive. It’s simple stuff.

And then there’s the BVM — aka the bag-valve-mask or “Ambubag.” Ask a room full of novice EMTs and they’ll all agree it’s about as straightforward as tying your shoes: slap it on, squeeze, any idiot could do it. But ask the senior medic in the corner, and he may paint a grimmer picture. Jeff Guy has described it as a more difficult skill than endotracheal intubation, yet one of the hot topics today in prehospital medicine is whether paramedics should remove intubation from their scope of practice because it’s too hard. But nobody’s going to take away the BVM. It’s irreplaceable; it’s the first and last line, the means of ventilation that any patient starts with, and the fallback if your next move fails. The only problem is that doing it well, and for really tough patients, doing it at all, is a purely skill-based exercise. It’s the Jedi’s lightsaber: simple, versatile, but designed for an expert.

The point is that establishing a patent airway in a sick person who can’t do it themselves, and ventilating them using that airway, is such an important task that it generally mandates a large toolbox. Airways are often managed via complex flowcharts or algorithms, where one method can yield to another if it fails, and then to another and another. Countless different devices and methods are available, so that even when obstacles are present, any moron can stumble onto something that works before the patient crashes altogether.

And then there’s us. The Basic EMT stands at the bottom of the spectrum in terms of training, yet is expected to oxygenate any patient using nothing but the meager BLS jump-kit. He has the BVM, a couple of basic airways, masks, cannulas, suction, positioning — and beyond that, just his wits and skills. And as for those, he probably spent little to no time actually practicing them in class, and may perform them only rarely in the field.

This won’t do. When it comes to psychomotor skills, these are the most essential, because we don’t have a Plan B. If BLS techniques fail, our only recourse is to sprint for the hospital or ALS, and hope nobody dies along the way.

So let’s talk about all the principles and tricks of creating a BLS airway and ventilating with the BVM. First, we’ll need to understand why it’s hard.

Basic Physiology

Ordinarily, we suck at breathing.

I mean we literally suck. We drop the diaphragm and widen the ribs, expanding the area inside our chest. This expands the lungs, forcing them to suck air into the only opening available — through the mouth and nose, down the pharynx, through the trachea, and into the bronchial tree.

That’s assuming that the airway is open, of course.

Now, what if I whack you over the head, and your body loses the ability to spontaneously breathe? We’ll want to breathe for you. Can we pull down your diaphragm and expand your chest? Not very easily, unless we stick a plunger on your sternum, or put you in an iron lung. Instead, we reverse this process: rather than creating negative pressure inside the chest, we force positive pressure in from the outside. Rather than sucking, we blow.

Blowing is a little tricky, though. One of the main problems is that there’s more than one place for air to go. Consider the pharynx, the working area of your upper airway. We can get there via two paths: the oropharynx (via the mouth and over the tongue), or the nasopharynx (via the nostrils), but they arrive at the same place, the laryngopharynx (or hypopharynx). What happens next?

If we peered into your hypopharyngeal space, we would see that two openings emerge below. One leads to a tube which lies posterior (toward your back): your esophagus, which conveys cheeseburgers and beer into your stomach. One leads to a tube which lies anterior (toward your front): your trachea, which brings air into the lungs for gas exchange. Remember these relative positions — the trachea is in front, and you can palpate it at the neck (the “Adam’s apple” is part of it). The esophagus lies behind this, and is not usually externally palpable.

Given that food and air both enter via the pharynx, how do we ensure that cheeseburgers ends up in the esophagus and air ends up in the trachea? Well, the gatehouse to the trachea is the larynx (the “voicebox,” where vocalization occurs), and the opening to this chamber is called the glottis. The glottis is normally open, but when you swallow, a couple of drape-like vestibular folds and a little flap, the epiglottis, are pulled in to cover the larynx. The result is that food is forced into the esophagus.

What about the other direction? The esophagus is formed from rings of muscles called esophageal sphincters, which help “milk” food downward when you swallow. The bottommost ring is the lower esophageal sphincter, which opens during swallowing, but otherwise is mostly constricted, sealing off the esophagus from the stomach itself. This prevents air from passing down and gastric contents from coming up (something we know as heartburn).

To summarize, as you sit here reading this, your esophagus is clamped off by your lower esophageal sphincter, and your trachea is open, allowing you to breathe. But if you take a bite of your coffee-cake, your epiglottis and vestibular folds will block off your airway, your esophageal sphincter will open, and the food bolus will be directed into your stomach.

Down the wrong pipe

The trouble with blowing instead of sucking is that we have no way of aiming where we blow.

I know what you’re thinking. If we force air down the pharynx, the esophageal sphincter should block off the stomach, ensuring that it flows into the larynx and down the trachea. Right?

Here’s the problem. Even ordinarily, your esophageal sphincter only clamps down with a small amount of force — say around 30 cmH2O (centimeters of water, a unit of pressure). This is plenty to prevent air from flowing in during regular respiration. But if air were to be pushed in with greater than 30 cmH2O of force, it will squeeze past the sphincter and enter the stomach. And if we clamp a BVM over your face and squish the bag, we can easily exceed that much pressure.

It gets worse. In order for the esophageal sphincter to work even that well, it requires muscular tone (constant stimulation), just like your postural muscles need tone to keep you from falling over. What happens when you’re unconscious? Sphincter tone decreases. So in the people we’ll actually be bagging, opening pressure may be 20–25 cmH2O or even less. Thus it’s even easier for positive pressure ventilations to force their way into the stomach.

The result? When squeezing the BVM, air often enters the stomach along with (or instead of) entering the lungs. Not only is this pointless, it makes it even harder to inflate the lungs (a bigger abdomen creates pressure on the diaphragm), decreases cardiac preload, and increases the risk of vomiting — which will further obstruct the airway.

The easiest solution is to put a tube into the trachea and seal it off — i.e. endotracheal intubation (or variations on that theme, such as a blind airway). Then we can blow air directly into the lungs without any chance that it’ll enter the wrong pipe. Unfortunately, those are tools we often lack as BLS providers.

Angles and Tissues

All of those structures we’ve been describing? They’re soft.

Soft and squishy. And it’s not just the esophageal sphincter that loses tone when you become unconscious.

In ordinary circumstances, the airway is a supple but structured arrangement of tissues that maintains its form. This is important, because there’s not very much space in there. So in the unresponsive patient, it’s no surprise that some of those tissues might collapse together, blocking off the lumen between them. (Check out this fluoroscopic video.)

The tongue is the worst. Tongues are basically big blobby muscles, attached at only one end, and if you remove all firming tone, they just flop wherever gravity takes them. So put an unconscious person supine, and gravity pulls the tongue back into the pharynx, blocking all airflow.

Or the larynx and supralaryngeal tissues run into the posterior pharyngeal wall. Or the soft palate does. Either way, anterior structures end up touching posterior structures, leaving no room in between. Our airway involves a tight 90 degree turn, and this is not a design that remains open without active maintenance. So if we want to breathe for these people, we need to find a way to unblock everything. (Like the jaw thrust — check out this airway cam.)

Mask Madness

Trying to push air into someone’s lungs by holding a mask over their face is like trying to blow up a tire by… well, holding a mask over the valve.

I teach CPR, and I can count on one hand the number of times I’ve handed the BVM to somebody and watched them achieve chest rise on the mannequin the first time. Heck, I demo the things and I don’t always pull it off.

Effectively sealing an air-filled plastic mask to someone’s face and then squeezing the bag is a task meant for more hands than any human possesses. Doing it on somebody who’s dying is exponentially more difficult. Add in the fact that they’re probably obese, toothless, vomiting, crumpled in a corner or bouncing around an ambulance, and enshrouded in a thick ZZ Top beard. Now try to get it all done without losing your cool or breaking your proper ventilatory rate. Having fun yet?

Key points

BLS ventilation using basic airways, positioning, and the BVM is a difficult, complex, and undertrained skillset for the EMT-B. Yet since we often lack rescue devices or alternate ventilation methods, it is critical that we learn to master it.

Preventing gastric inflation would be difficult even in healthy people, and is extremely difficult in the apneic and unresponsive patient.

We all have some idea what shock looks like. Like many pathologies, its loudest early markers are actually indirect — we’ll often recognize the body’s reactions to shock rather than the shock itself.

Although there are a few ways to classify the stages of shock, let’s just use three categories here.

Early or Insignificant

Shock that is very early or minimal in effect may have no particular manifestations. One situation where significant or late shock may also be “hidden” is in the elderly patient, or anyone with significant comorbidities; if their body’s ability to mobilize its compensatory mechanisms is poor, then the red flags won’t be as obvious. This doesn’t mean the shock isn’t as bad; in fact, it means that it’s worse, because their body can’t do as much to mitigate it.

The way to recognize shock at this stage is from the history. If we see an obvious bullet hole in the patient’s chest, and three liters of blood pooling on the ground beside him, then it doesn’t matter how the patient presents otherwise; we’re going to assume that shock is a concern. Blood volume is proportional to bodyweight, but for a typical adult, a fair rule of thumb is to assume about 5-7 liters of total volume. (Not sure what a liter looks like? The bags of saline the medics usually carry are a liter; so are those Nalgene water bottles many people drink from. “Party size” soda bottles are two liters.) Losing more than a liter or two rapidly is difficult to compensate for.

Remember, of course, that blood can also be lost internally, and aside from the occasional pelvic fracture or hemothorax, the best environment for this is the abdomen. Always examine and palpate the abdomen of the trauma patient, looking for rigidity, tenderness, or distention. Remember also that the GI tract is a great place to lose blood; be sure to ask your medical patients about blood or “coffee grounds” (old blood) in the vomit or stool.

Fluid enters and leaves the body continuously, and any disruption in this should be recognized. If a patient complains “I haven’t been able to eat or drink anything in two days,” they’re telling you that they haven’t taken in any fluid for 48 hours. If they tell you they’ve been vomiting or experiencing profuse diarrhea, that’s fluid leaving their body in significant volumes. What about the man who just ran a marathon and sweated out a gallon? Did he drink a gallon to replace it?

Compensated Shock

Significant shock will result in the body attempting to compensate for the low blood volume. Much of this work is done by the sympathetic system, and there are two primary effects: vasoconstriction and cardiac stimulation.

By constricting the blood vessels, we can maintain a reasonable blood pressure and adequate flow even with a smaller circulating volume. We normally vasoconstrict in the periphery — particularly the outer extremities and skin — “stealing” blood from those less-important tissues and retaining it in the vital core. This causes pallor (paleness) and coolness of the external skin. The sympathetic stimulation may also cause diaphoresis (sweating), which is not compensatory, but simply a side effect of the adrenergic release.

The heart also kicks into overdrive, trying to keep the remaining volume moving faster to make up for the loss. It beats faster (chronotropy) and harder (inotropy), resulting in tachycardia. Note that patients who use beta blockers (such as metoprolol) may not be able to muster much, if any, compensatory tachycardia.

A narrowing pulse pressure (the difference between the systolic and diastolic numbers) may be noted; since the diastolic reflects baseline pressure and the systolic reflects the added pressure created by the pumping of the heart, a narrow pulse pressure suggests that cardiac output is diminishing (due to loss of preload), and that more and more of the pressure we’re seeing is simply produced by shrinking the vasculature.

Tachypnea (rapid respirations) are also typically seen. In some cases, this may be due to emotional excitement, and there is also a longstanding belief that it reflects the body’s attempts to “blow off” carbon dioxide and reduce the acidosis created by anaerobic metabolism. (Interestingly, lactate — a byproduct of anaerobic metabolism — can be measured by lab tests, and is also a sign of shock, particularly useful in sepsis.) Additionally, it ensures that all remaining blood has the greatest possible oxygenation. However, it is also plausible that this tachypnea serves to assist the circulatory system: by creating negative pressure in the thorax (the “suction” you make in your chest whenever you inhale) and positive pressure in the abdomen (due to the diaphragm dropping down), you “milk” the vena cava upward during inspiration, improving venous return to the heart and allowing greater cardiac output. This “bellows” effect helps the heart fill more and expel more with each beat.

The more functional the patient’s body is — such as the young, strong, healthy victim — the more effective these compensatory systems will be. Hence the old truism that pediatric patients “fall off a cliff” — they may look great even up through quite profound levels of shock, due to their excellent ability to compensate, then when they finally run out of room they’re already so far in the hole that they become rapidly unhinged. It’s great that these people can compensate well, but it does mean we need to have a high index of suspicion, looking closely for signs of compensation (such as tachycardia) rather than outright signs of shock — because by the time the latter appears, it may be very late indeed.

Patients in compensated shock may become orthostatic; their bodies are capable of perfusing well in more horizontal postures, but when gravity pulls their remaining blood away from the core, this added challenge makes the hypovolemia noticeable. Less acute shock due to causes like dehydration may result in dry skin (particularly the mucus membranes; try examining the inside of the lower eyelid) with poor turgor (pinch a “tent” out of their skin and release it; does it snap back quickly or sluggishly?), and potentially with complaints of thirst. Urine output will usually be minimal. Generally, the more gradually the hypovolemia sets in, the more gradually it can be safely corrected; it’s the sudden, acute losses from causes like bleeding that we’re most worried about.

Decompensated Shock

As shock continues, compensatory systems will struggle harder and harder to maintain perfusion and pressure. Eventually they will fail; further vasoconstriction will reduce rather than improve organ perfusion, beating the heart faster will expel less rather than more blood, and the blood pressure will start to drop.

The hallmark of this stage of shock is the normal functioning of the body beginning to fail. The measured blood pressure will decrease and eventually become unobtainable. Pulses will weaken until they cannot be palpated. As perfusion to the brain decreases, the patient’s mental status will deteriorate. Heart rate and respirations, previously rapid, will begin to slow as the body loses the ability to drive them; like a government office that can’t pay its workers, the regulatory systems that should be fighting the problem begin to shutter their own operations. As the heart continues to “brady down,” eventually it may lose coherence (ventricular fibrillation), or keep stoically trying to contract until the last, but lose all effective output due to the lack of available blood (PEA). Cardiac arrest ensues, with dismal chances for resuscitation.

Alternative Forms of Shock

Although we have focused so far on hypovolemic shock, particularly of traumatic etiology, there are other possibilities. A wide range of shock types exist, but speaking broadly, there are only two other categories important to us: distributive, and cardiogenic/obstructive.

Distributive shocks include anaphylactic, septic, and neurogenic. The essential difference here is that rather than any loss of fluid, the vasculature has simply expanded. Rather than squeezing down on the blood volume to maintain an appropriate pressure, the veins and arteries have gone “slack,” and control of the circulating volume has been lost; it’s simply puddled, like standing water in a sewer pipe. (Depending on the type of shock there may also be some true fluid losses due to edema and third-spacing.) Imagine tying your shoes: in order to stay securely on your feet, the laces need to be pulled snugly (not too tight, not too loose). If the knot comes undone and the laces lose their tension, the shoe will likely slip right off. Your foot hasn’t gotten smaller, but the shoe needs to be hugging it properly to stay in place, and it’s no longer doing its job.

The hallmark of distributive shock is hyperemic (flush or highly perfused) rather than constricted peripheral circulation. The visible skin is warm (or hot) and pink (or red), and the patient may be profoundly orthostatic. Septic shock is associated with infection; anaphylactic with an allergic trigger; and neurogenic with an injury to the spinal cord.

Cardiogenic and obstructive shocks are a different story. In this case, there’s nothing wrong with the circulating volume, or with the vasculature it flows within; instead, there’s a problem with the pump. Cardiogenic shock typically refers to situations like a post-MI heart that’s no longer pumping effectively. Obstructive shock refers to the special cases of pericardial tamponade, massive pulmonary embolism, or tension pneumothorax: physical forces are preventing the heart from expanding or blood from entering it, and hence (despite an otherwise functional myocardium) it’s unable to pump anything out. In either case, we can expect a clinical picture generally similar to hypovolemic shock, but likely with cardiac irregularities — such as ischemic changes or loss of QRS amplitude on the ECG, irregularity or slowing of the pulse, or changes in heart tone (such as muffling) upon auscultation. Pulsus paradoxus (a drop in blood pressure — usually detected by the strength of the palpable pulses — during the inspiratory phase of breathing), electrical alternans (alternating QRS amplitudes on the ECG), and jugular vein distention also may be present in the case of tamponade or severe tension pneumothorax.

In sum, remember these general points:

The history and clinical context should be enough to make you suspect shock even without other signs or symptoms.

The faster the onset, the more urgent the situation; acute shock needs acute care.

Look both for signs of compensation (such as tachycardia) and for signs of decompensation (such as falling blood pressure). However, remember that due to confounding factors (such as particularly effective or ineffective compensatory ability, or pharmacological beta blockade), any or all of these may be absent.

This past weekend, I was able to attend the Western Massachusetts EMS Conference alongside such luminaries as Scott Kier and Kyle David Bates (of the extraordinary Pedi-U podcast). We sat through two days of outstanding lectures on various EMS-related topics, and walked away with some ideas and information I haven’t found anywhere else. Here are just a few of the unique pearls from the conference. Thanks to everyone for the great time!

Kyle David Bates on Mechanism of Injury

In an MVC, ejected (that is, fully ejected) victims have a 1/3 chance of a cervical spine fracture.

They also have around 25 times higher chance of mortality than an equivalent non-ejected patient.

Is “another death in the same vehicle” a legitimate concern when considering mechanism? Yes, but make sure that death wasn’t from an localized cause—for instance, a girder in the face, or they had a heart attack before they crashed.

How about “intrusion”? Over twelve inches into the patient compartment where your patient is found (meaning, visible from inside—not from the outside, which includes the buffer space of the walls), not including areas like the hood, trunk, etc. Alternately, over 18 inches into the patient compartment in areas where your patient is not found—for instance, the rear seating area, when you’re treating the solo driver.

“Distracting injuries” can mean painful injuries that distract the patient, but also gross stuff that distracts the provider. Consider a head-to-toe on virtually everyone, even when the funky arm fracture is drawing your attention.

Many “trauma” patients are no longer being treated with surgery anyway, so sending everything to the trauma centers overloads them for no reason.

One more reason why the sternal rub is not a great diagnostic: if they do clutch at their chest in response, is that localizing—or an abnormal, decorticate flexion response? Different GCS scores, but you can’t tell.

Are extremity injuries significant mechanisms? Penetrating injury proximal to the elbows or knees should be considered threatening to the torso, so yes. Pelvic fractures? For sure. (“How much blood can you lose into your pelvis? All of it!”)

With the automobile safety technology available today, you can crash fast, turn your car into a paperweight, but walk away unharmed. We no longer care about “high-speed,” only “high-risk,” which has many factors (see the Rogue Medic’s recent post on this).

Auto vs. pedestrians: kids get upper body injuries; adults get lateral trauma as we turn and try to get out of the way. Both can get run over.

Motorcycles. Harley-type riders seem to have more head injuries: they get hit by cars, due to low profile and dark clothing, and they wear partial helmets. Sports bikes get more extremity injuries: they wear good protection, are higher visibility, but they ride fast and run into things, breaking any and every bone they have.

Rollovers: no longer trauma criteria. You can roll and do great if you’re restrained. Number of rolls, final position, even roof intrusion have no correlation to injury severity.

Extrication time >20 minutes: no longer trauma criteria. Sometimes it just takes a while due to weather, access, etc, and newer vehicles are supposed to crumple more anyway.

Are burns trauma criteria? No. If they need specialized care, it’s a burn center, but this is not that time-sensitive—more a long-term management thing—so someone with burns and trauma should go to the trauma center instead, can be transferred later for burn care.

Helicopter transport: costs can range from $2,000 to $20,000 depending on distance, and insurers are refusing to pay many of these bills due to lack of necessity. Also consider the possibility of everyone dying in a fiery crash. Weigh cost vs. benefit.

Kyle David Bates on Shortness of Breath

Anxiety is caused by hypoxia; the cure for this is supplemental oxygen.

Sleepiness is caused by hypercapnia; the cure for this is bagging.

OPA or NPA? Testing the gag reflex may create a bigger airway problem (vomit). Better yet, check the mouth for pooled saliva; if present, there is no gag, use an OPA. If absent, they have a gag and are managing their own secretions, use an NPA.

Pulsus paradoxus/paradoxical pulses are a useful early sign of significant pulmonary dysfunction.

90% of asthma attacks linked with an allergic reaction; however, rhinovirus (the common cold) may now be a contender. Others include: exercise (not sure why; maybe the temperature differential), active menstruation (asthma very common in young post-pubescent women—maybe the hormones), psychological (stress, panic), aspirin use.

Kids compensate great, so cyanosis (a decompensation sign) in kids is very late and very bad.

Risk-stratify these patients, because high risk patients can decompensate fast even if they look okay now. Previous hospitalizations? ICU admits? Intubations?

Cough asthma: no dyspnea, just dry coughing. It happens.

Smokers: measured in pack-years. 1 pack a day for 20 years is 20 pack-years, 2 packs a day for 5 years is 10 pack-years; 30–35 pack-years is where we start to see bad dysfunction.

Best place to check skin? Under the lower eyelid—lift it and check the mucus membranes. Dry for dehydration, pale for shock, blue for cyanosis, the whole gamut.

Nebulized ipratropium/Atrovent: its role is mainly to reduce mucus and secretions (cf. atropine). Tachycardia etc. is not a contraindication, because it’s not absorbed systemically; it remains in the lungs.

Give nebs by hand-held mask or T-piece instead of strapping it to their face; that way you have a warning of deterioration when they can no longer hold it to their face.

Bronchodilators may not work great in beta-blocked patients.

Steroids take hours to have an effect, but the earlier they’re given the better the outcomes; give ’em if you have ’em.

If they need RSI, ketamine is nice because it also bronchodilates.

“Facilitated intubation” (i.e. snow ’em with a ton of benzos/narcs)? Be careful, because if you don’t get that tube, it’ll take forever to wear off; these aren’t short-duration drugs.

Kyle David Bates on Pediatrics

Use the Pediatric Assessment Triangle! Appearance, Work of Breathing, Circulation.

Airway: crying is a great sign. Remember to pad under the shoulders when lying flat, their huge heads can tip them forward and block the airway. Avoid NPAs in infants. In very small kids, breath sounds can transmit, so you may hear upper sounds in the chest or chest sounds in the trachea.

Under 2 months: peripheral cyanosis is normal, central cyanosis is bad. Limited behavior, often won’t visually track. Ask parents if their behavior is normal. Ask about obstetric history, it’s still relevant. They have no immune system really, so any infection (temp over 100.4) is a serious emergency.

2–6 months: social smile, will track visually, recognize mom, strong cry and can roll/sit with support. May still be okay with strangers, but try to keep them with parents; if parents like you, they’ll like you

6–12 months: stranger anxiety (unless they’re raised very communally). Very mobile and explore with their mouth, so always think about foreign body airway obstructions, especially up the nose, especially for dyspnea with sudden onset. Separation anxiety, so keep with parent. Offer distractions (toys, etc.). Do exam from toe to head so they get used to you before you reach their face.

1–3 yrs (toddlers, “terrible 2s”): mobile, curious, opinionated, ego-centric, can’t abstractly connect cause-and-effect but learn from experience. Keep with the parents, distract them, assess painful part last (or everything you touch afterwards will hurt). May talk a lot or not much, it’s all normal, but they always understand more than they let on, so be careful what you say.

3–5 yrs (preschool): magical thinkers, misconceptions (“silly” ideas like if they leak too much they’ll run out of blood), many fears (death/darkness/mutilation/aloneness), short attention span. Explain things in simple terms, relate to them (any cartoons or toys in the house you recognize?), use toys, involve them (here hold this, which arm should I use, etc). Don’t ever negotiate, just tell them what to do; praise them often; never ridicule.

6–12 yrs (school aged): talkative, mobile, may not get cause and effect, want reassurance, involvement, praise. Live in present, may not think about danger or risk. Peer involvement. Speak directly to them, anticipate questions (will this hurt? am I going to die?), give simple explanations, don’t ever lie, respect privacy. If you need to do something painful (IVs, etc.) don’t tell them until just before, or they’ll dwell on it. Head-to-toe okay.

13–18 (adolescents): regress when hurt or sick—act like big toddlers. Can understand and theoretically have common sense, but still take risks. Peer support. Speak directly, give concrete explanations, respect privacy, have patience.

Under 21 usually considered “pediatric.”

Degree of fever temp not associated with severity. No actual danger to brain until 106–107 degrees F or so.

Dr. Lisa Patterson on Trauma and Field Triage

RR <20 in infants is trauma center criteria since this is the one easily-measurable vital sign for them.

Crushed/degloved/mangled extremities: although not life-threatening, still worth the divert, because usually needs multi-specialty care (plastic surgery, orthopedics, hand specialists, etc.) to maximize function.

Calling in “altered mental status” or “unresponsive” is not super helpful—give a GCS or otherwise specify what you mean, there’s a big range here.

Trauma activations here are typically three tiers: category 1 (life threat), category 2 (no immediate emergency, but some concern or suspicion due to mechanism or presentation), consult (no concern on initial presentation, but later decision to admit, trauma paged down to consult).

Sean Dorr on OEMS investigations

[This is Massachusetts-specific information; local providers can contact me directly if they want to hear about some of this material.— ed.]

Ginnie Teed on Organ and Tissue Donation

Donation is hugely hugely valuable and lifesaving, but there’s not nearly enough. About 60-70% of Americans are registered donors, around 100 million people, but only 1% end up as usable donors and we need far more. Low rates aren’t from consent, they’re from the logistics of getting viable candidates.

Uniform Anatomical Gift Act (UAGA) is federal regulation providing basic requirements for process; states use this standard to form their own systems. Registered donors must be recognized and organ procurement agencies are required to advocate for them even against wishes of family, etc. Driver’s license “opt-in” now considered legal consent in some but not all states.

National Organ Transplant Act establishes the rules of the registry, blinds the entire process, prevents manipulation or line-jumping; the database is centralized and controlled; you can’t legally buy or otherwise get around the system. Manipulation is taken very very seriously and massively investigated, because it’s not only unethical, the pall it casts over the process makes others decide not to donate—the result is many lives lost.

Tissues used: not living, usually good for about 24 hours after death. Bones (not marrow, which is living), although we try to not obviously mutilate people (for their family’s sake), skin (hugely beneficial), corneas, vessels, heart valves, pericardium, connective tissue (for orthopedic repairs).

Three ways to declare death: neurological (no brain activity; body only alive due to our mechanical support; recovery team responds to site and performs planned recovery); cardiac death (heart stops; not planned); planned extubation/cardiac death (patient is mechanically supported, determination made that there is no possibility to survive on their own; vent is pulled, if heart stops within 59 minutes they can take some organs; usually just the durable liver and kidneys unless bypass is available).

Live organs can only be taken from perfused patients. Someone “dead” (i.e. no pulses) can be a tissue donor but not an organ donor unless you get ROSC. No point in continuing CPR to “maintain the organs” if there’s no possibility of getting return of circulation.

EMS documentation absolutely critical for determining donor eligibility. Need to know downtime in arrests, how much CPR, any ROSC no matter how brief, events/mechanism leading to arrest. There are hard limits on fluid/blood/colloids received, so they must know how much fluid you gave (reasonable estimate is fine). Must document all needlesticks, number and location; if they find any holes that aren’t accounted for they’ll have to assume they’re a drug user or that additional lines were started and extra liters given. If you don’t want to document something at least tell the receiving staff.

If blood is drawn, label must be placed so that expiration date of tube is still readable (FDA requirement).

Every donor can save up to 200 people; failure to document can kill just as many.

UMass Memorial LifeFlight on Air Ambulance Transport

Consider: how do you want the helicopter used? Need their higher level of care? Rapid transport to trauma center? Transport multiple patients in an MCI to more distant hospitals to reduce burden on closest facilities? Can even split the crew to provide higher level of care for multiple ground ambulances.

Many services simply will not fly into a hazmat situation.

Best makeshift landing zones are schools—big open areas, everyone knows where it is.

Wires are a major hazard, make sure to warn pilot—you can see them but he can’t.

Need about 100 x 100 ft for an LZ, or 35–40 big-ish strides per side. Secure the area against bystanders.

Bad surfaces are dust, dirt, snow, ice, hay. Snow should ideally be very fluffy or very packed. If they land and get iced they may not be able to take off again. Don’t wash down a dusty LZ unless pilot requests it. Paved areas are simplest and best. Large clear roadways can land multiple choppers in a row.

Lighting options: orange traffic cone at each corner, with a handlight placed in each at nighttime. Or, flashing ministrobe at each corner. Or, vehicle headlights crossing the LZ. Don’t shine anything up at the helo, don’t mark with loose material, don’t use flares.

Designate one person as LZ Command (not the IC). Nobody else communicates with the helicopter. Your portable radio probably won’t reach them; use the mobile in the truck. If there’s any hazard on final approach, say one word—”STOP”—and pilot will abort.

Most crashes are pilot error, and most pilot error is due to fatigue. There should be hour limits for a pilot, and this is a valid reason to refuse to fly.

Detective John LeClair, EMT-P, on Opiates and Prescription Pills

Heroin is still big, but pills are a huge player now too. You get an easy prescription from a walk-in clinic or ED, pay maybe a couple bucks with Medicare/Medicaid, and can not only sell them for easy cash but can crush and snort/shoot it for the same effect as heroin. Then if money or access runs low, you end up on heroin anyway to chase that high.

Oxycontin/oxycodone best selling narcotic in the nation ten years ago, but now on the wane. You scrape off the time-release coating, crush it and snort or chew it. “Hillybilly heroin,” “blue,” “oxycotton,” “kicker,” etc. Street price about $1/mg (40mg, 80mg, 160mg common), so many turned to crime. In Aug 2010, manufacturer (Purdue) added a “geling” agent which turns it to gel when it contacts water, making it difficult to snort. Try to snort this Oxycontin OP and it turns into a ball in your nose. Some people are sticking straws/tubes up in there to try and get it deeper and deeper, so airway obstructions are happening.

Percocet: oxy plus acetaminophen. For years the most common analgesic for sports injuries, so common among youth. Kids shared ’em, put out bowls of them at parties, girls prostituted themselves for pills. Taken with alcohol the APAP/Tylenol kills your liver. “Littles,” “little babies,” “little dogs.”

Opana/oxymorphone: getting popular after Oxy OP started ruining everyone’s fun. Same idea but you can still snort it. Twice as strong, and costs twice as much ($2/mg)

How to grind? Take a hose clamp, cut it, straighten it, tape it down, run the pill across the holes to grind it. Or use a Pedi-Egg, which collects the powder for you. The finer, the better high.

Heroin: snort, “skin pop” (subcutaneous), mainline. Must be pretty pure to snort, which it now tends to be, so popularity grew (people were afraid of needles due to HIV). However now some HIV/Hep is spreading through bloody noses and sharing straws anyway.

Heroin addicts are creatures of habit; get high same place, same way. Any change in their routine (e.g. different location) can get them amped up, changing their sensitivity and leading to OD even with their usual dose. Consider this if you find an OD somewhere like a car or alley.

“Cotton fever”: they pluck out wads of cotton from cigarette filters and drop it in the heroin to help filter it. Sometimes when they draw out the liquid they get a bit of cotton, and when they shoot it they get a sort of phlebitis/infection/sepsis.

Pulse oximetry is not always available in EMS — depending on level of care, scope of practice in your area, and how your service chooses to equip you — but when it is, it’s a valuable tool in your diagnostic toolbox. Just like we discussed before, and just like any other piece of the patient assessment, using it properly requires understanding how it works and when it doesn’t.

Clinical context: When a sat is not a sat

Simply put, oximetry is the vital sign of oxygenation. It is the direct measurement of the oxygen in your bloodstream. It does not quite measure the oxygen that is actually available to your cells, but it gets close.

First, remember that actual oxygen delivery requires not just adequate hemoglobin saturation, but also enough total hemoglobin, moving around at an adequate rate. In hypovolemia, such as the shocky trauma patient, or in anemia, you might see a high SpO2 — which may be entirely accurate — but this doesn’t necessarily mean that the organs are not hypoxic. After all, you could have nothing but a single lonely hemoglobin floating around, and if it had four oxygen bound to it, you would technically have a sat of 100%. But that won’t keep anyone alive. Evaluating perfusion is a separate matter from evaluating oxygenation.

Second, remember our discussion of the oxyhemoglobin dissociation curve. The fact that you have oxygen bound to your hemoglobin doesn’t mean that it’s actually being delivered to your cells. That is, you can be hypoxic — inadequate cellular oxygenation of your organs — without being hypoxemic — inadequate oxygen present in the blood. Oximetry will only reveal hypoxemia.

Two of the strongest confounders here are cyanide and carbon monoxide (CO) poisoning. The main effect of cyanide is to impair the normal cellular aerobic cycle, preventing the utilization of oxygen; since it has no effect on your lungs or hemoglobin, the result is a normal saturation, yet profound hypoxia, since none of the bound oxygen can actually be used. Carbon monoxide, on the other hand, involves a twofer; it binds to hemoglobin in the place of oxygen, creating a monster called carboxyhemoglobin. CO has far more affinity for carboxyhemoglobin than oxygen does, so it’s hard to dislodge, and you therefore lose 1/4 of your available binding sites in the affected hemoglobin. But it doesn’t stop there. Carboxyhemoglobin also has a higher affinity for oxygen. This creates a leftward shift in the oxyhemoglobin dissociation curve — the oxygen that actually does bind finds itself “stuck,” and these well-saturated boats happily sail past increasingly hypoxic tissues without ever unloading their O2.

Consider the oximetric findings in these patients. The cyanide patient will have unimpaired blood oxygenation, so (unless he has already succumbed to respiratory failure due to the effects), a normal sat will be seen; however, hypoxia will be clinically apparent, particularly as ischemia of the heart and brain. Carbon monoxide, on the other hand, will reveal a normal or elevated (100%) sat which is partially accurate — some of that is true oxygen — and partially baloney, since CO looks the same to the oximeter as O2. But this is moot, because neither the bound CO nor the bound O2 is available to the cells. Oximeters do exist that can detect the presence of carboxyhemoglobin, known as CO-oximeters, but they are expensive and uncommon, and there is some question as to their accuracy. Your best helper here is in the patient history: both CO and cyanide are produced by fires, or any combustion in enclosed spaces (such as stoves or heaters), cyanide being released by the combustion of many plastics. You should be very wary of normal sats in any patient coming from a house fire or similar circumstances.

(Both cyanide and CO poisoning are known for causing bright red skin. In both cases oxygen is not being removed from hemoglobin, so arterial blood remains pink and well-saturated. Carboxyhemoglobin itself is also an unusually bright red. This skin, a late sign, is usually seen in dead or near-dead patients.)

Third, consider that although oximetry is an excellent measure of oxygenation, this is not the same as assessing respiratory status. It’s a little like measuring the blood pressure: although it’s a very important number, BP is an end product of numerous other compensatory mechanisms, and a normal pressure doesn’t mean that there aren’t challenges being placed on it — merely that they’re challenges you’re currently able to compensate for. Perhaps you’re satting 98%, but only by breathing 40 times a minute, and you’re fatiguing fast. Perhaps you’re satting 94%, but your airway is closing quickly and in a few minutes you won’t be breathing at all. These are clinical findings that may not be revealed in SpO2 until it’s too late.

Fourth: oximetry measures oxygenation, but not ventilation. When you breathe in, you inhale oxygen; when you breathe out, you exhale carbon dioxide. Although we use the term ventilation to describe the overall process of breathing, formally in the respiratory world it refers to the removal of carbon dioxide. Is oxygenation the more important of these two functions? Certainly; it will kill you much faster. But hypercapnia (high CO2) caused by inadequate ventilation is also a problem, and pulse oximetry does not measure it. (Capnography is the vital sign of ventilation, but that’s a topic for another day.) Now, insofar as oxygenation is primarily determined by respiratory adequacy (rate, volume, and quality of breathing), and respiration both oxygenates and ventilates, oximetry can be a good indirect measurement of ventilation; if you’re oxygenating well, you’re probably ventilating well too. This remains true if breathing is assisted via BVM, CPAP, or other device. But this is not true if supplemental oxygen is applied. Increasing the fraction of inspired oxygen (FiO2) improves oxygenation without affecting ventilation; on 100% oxygen I might be breathing 8 times a minute, oxygenating well, but ventilating inadequately.

Finally, it’s worth remembering that once you reach 100% saturation, PaO2 may no longer correlate directly with SpO2. If you reach 100% saturation at a PaO2 of 80, we could keep increasing the available oxygen until you hit a PaO2 of 500, but your sat will still read 100%. So without taking a blood gas, we don’t know whether that sat of 100% is incredibly robust, or is very close to desatting. (That’s not to say that a higher PaO2 is necessarily better; recent research continues to suggest that hyperoxygenation is harmful in many conditions. Not knowing the true PaO2 can be problematic in either direction.)

Hardware failure: When a sat is not anything

In what clinical circumstances does oximetry tend to fail? The primary one is when there isn’t sufficient arterial flow to produce a strong signal. This can be systemic, such as hypovolemia — or cardiac arrest — or it can be local, such as in PVD. (The shocked patient has both problems, being both hypovolemic and peripherally vasoconstricted.) Feel the extremity you’re applying the sensor to; if it’s warm, your chances of an accurate reading are good. The best confirmation here is to watch the waveform; a clear, accurate waveform is a very good indicator that you have a strong signal.

Tremors from shivering, Parkinsonism, or fever-induced rigors can also produce artifact on the oximeter. Some patients also just don’t like the probe on their finger. Try holding it in place, keeping the sensor tightly against the skin and the digit motionless. If there’s no luck, try another site. Any finger will work, or any toe, or an earlobe. (Some devices don’t require “sandwiching” the tissue, and can be stuck to the forehead or other proximal site, but these are uncommon in outpatient settings.)

There are a few other situations that can interfere with normal readings. In most cases, nail polish is not a problem, but dark colors do decrease the transmittance, so some shades have been reported to produce falsely low readings in the presence of already low sats or poor perfusion — as always, check your waveform for adequate signal strength. Very bright fluorescent lights have been reported to create strange numbers, and ambient infrared light — such as the heat lamps found in neonatal isolettes — can certainly create spurious readings. A few other medical oddities fall into this category as well, including intravenous dyes like methylene blue, and methemoglobinemia, which produces false sats trending towards 85%.

Is oximetry a replacement for a clinical assessment of respiration, including rate, rhythm, subjective difficulty, breath sounds, skin, and relevant history? Absolutely not. But since none of those actually provide a quantified assessment of oxygenation, they are also no replacement for oximetry. It is a valuable addition to any diagnostic suite, particularly to help in monitoring a patient over time, as well as for detecting depressed respirations before they become clinically obvious — especially in the clinically opaque patient, such as the comatose. When it’s unavailable in the field, we readily do without it. But when it’s available, it’s worth using, and anything worth using is worth understanding.